» I definitely understand that there is not literally a built-in doorway for
» injected material to get inside of follicles. I don’t mean it literally
» when I use the terms “opening” or “doorway” or “entry way”. I mean those
» terms in a virtual sense rather than a literal sense. I mean that the
» follicles have to have the right characteristics, including size, in order
» to receive and intake the cells. To give an extreme example, it would
» obviously be impossible for cells to get inside of follicles if the cells
» are larger than the follicles and the cells would not have to be larger
» than follicles in order to make penetration of the cells impossible.
But again, you’re talking about “get inside”. You denied you were talking about a “doorway”, but you’re still talking about “getting inside”.
I am telling you that your assumption that there’s any “getting inside” is off the mark.
The cells aren’t getting or going inside of anything. In fact, there really isn’t any “inside” at all.
If, after being injected, a cell happens to find itself close enough to a follicle to interact with the follicle chemically, perhaps by some chemoattractant agent, then it may adhere to the follicle and may adhere to the papilla of the follicle, and replenish the follicle in that way by simply adding to the mass and bulk of the follicle and becoming integrated with it.
All the cells are always the same size, so there is NO size barrier for any of this. You’re thinking too much and it’s obvious that you haven’t studied cell biology beyond a very elementary point. You’re creating all these assumptions and requirements that simply do not exist.
» I assumed that since in AGA the follicles are getting smaller, then that
» means that everything inside of the follicles, including the cells, are
» getting smaller. Are you 100% sure that I’m wrong about this???
OK, you know that I have studied cell biology at very advanced levels. I know of NOTHING, ever, in my study of cell biology that tells me that when an organ shrinks or is “resorbed” or atrophies, that the reason for this is a significant shrinkage in the size of the individual cells, as opposed to the numbers of cells.
There are sometimes situations where cells become a tiny bit smaller because they may no longer be engorged with some product. For instance, keratinocytes that were once producing a lot of keratin, might become a bit smaller if they’re no longer producing much keratin (although most of the keratin is sent outside the cell, anyway.) But the relative diminution in the size of these cells, compared to larger surrounding structures like the follicle itself, would be so negligible as to be irrelevant.
BUT… even if what you say is true, and it is not – it STILL would not have the effect you think!
So to me it’s not even worth thinking about, from square one. It’s a useless exercise in unscientific thought.
» » I definitely understand that there is not literally a built-in doorway
» for
» » injected material to get inside of follicles. I don’t mean it literally
» » when I use the terms “opening” or “doorway” or “entry way”. I mean those
» » terms in a virtual sense rather than a literal sense. I mean that the
» » follicles have to have the right characteristics, including size, in
» order
» » to receive and intake the cells. To give an extreme example, it would
» » obviously be impossible for cells to get inside of follicles if the
» cells
» » are larger than the follicles and the cells would not have to be larger
» » than follicles in order to make penetration of the cells impossible.
»
» But again, you’re talking about “get inside”. You denied you were talking
» about a “doorway”, but you’re still talking about “getting inside”.
»
» I am telling you that your assumption that there’s any “getting inside” is
» off the mark.
»
» The cells aren’t getting or going inside of anything. If, after being
» injected, a cell happens to find itself close enough to a follicle to
» interact with the follicle chemically, perhaps by some chemoattractant
» agent, then it may adhere to the follicle and may adhere to the papilla of
» the follicle, and replenish the follicle in that way by simply adding to
» the mass and bulk of the follicle and becoming integrated with it.
»
» All the cells are always the same size, so there is NO size barrier for any
» of this. You’re thinking too much and it’s obvious that you haven’t
» studied cell biology beyond a very elementary point. You’re creating all
» these assumptions and requirements that simply do not exist.
Wow! I stand corrected. I always assumed that since the follicles shrink in AGA that means that everything inside the follicles shrink (including the cells) in AGA. I didn’t bother looking to establish whether that is true or not because I assumed it and nobody has ever said anything to make me question it until now.
Well, now that I’m informed that the cells themselves do not shrink that bodes even better for the Aderans treatment being compoundable. I wonder why Aderans didn’t try follow/up injections at different intervals. Doesn’t it seem like they should try it in phase 3???
» Wow! I stand corrected. I assumed that since the follicles shrink in AGA
» then everything inside the follicles shrink (including the cells) in AGA. I
» didn’t bother looking to establish that because all of the illustrations
» show the follicles shrinking in AGA so I just assumed that the cells were
» also shrinking.
Well, now you know.
» Well, now that I’m informed that the cells themselves do not shrink that
» bodes even better for the Aderans treatment being compoundable.
I think it does, but I think that the compoundability issue is much more related to probability, relative distances and scale, and the statistical notion that if you keep repeating an event with X probability of success, the cumulative probability of success is basically the sum of all the individual probabilities. So if you roll a pair of dice 10 times, you have a 10X greater chance of getting at least one lucky 7, than if you roll the dice only once.
» I wonder why Aderans didn’t try follow/up injections at different intervals.
» » I assumed that since in AGA the follicles are getting smaller, then that
» » means that everything inside of the follicles, including the cells, are
» » getting smaller. Are you 100% sure that I’m wrong about this???
»
» OK, you know that I have studied cell biology at very advanced levels. I
» know of NOTHING, ever, in my study of cell biology that tells me that when
» an organ shrinks or is “resorbed” or atrophies, that the reason for this is
» a significant shrinkage in the size of the individual cells, as opposed to
» the numbers of cells.
»
» There are sometimes situations where cells become a tiny bit smaller
» because they may no longer be engorged with some product. For instance,
» keratinocytes that were once producing a lot of keratin, might become a bit
» smaller if they’re no longer producing much keratin (although most of the
» keratin is sent outside the cell, anyway.) But the relative diminution in
» the size of these cells, compared to larger surrounding structures like the
» follicle itself, would be so negligible as to be irrelevant.
»
» BUT… even if what you say is true, and it is not – it
» STILL would not have the effect you think!
»
» So to me it’s not even worth thinking about, from square one. It’s a
» useless exercise in unscientific thought.
Ok then. And thanks for clearling that up. And this makes the idea of doing follow-up injections at different intervals with the Aderans treatment even more attractive.
Keep in mind that Histogen got better results when they did follow-up injections. I think that the same thing could happen with Aderans. I understand that they are two different types of treatments so follow-up treatments might be effective with Histogen’s treatment but not with Aderans treatment, but I think it does seem plausible that the Aderans treatment could produce better results with follow-up objections.
» » Wow! I stand corrected. I assumed that since the follicles shrink in
» AGA
» » then everything inside the follicles shrink (including the cells) in AGA.
» I
» » didn’t bother looking to establish that because all of the illustrations
» » show the follicles shrinking in AGA so I just assumed that the cells
» were
» » also shrinking.
»
» Well, now you know.
»
»
» » Well, now that I’m informed that the cells themselves do not shrink that
» » bodes even better for the Aderans treatment being compoundable.
»
» I think it does, but I think that the compoundability issue is much more
» related to probability, relative distances and scale, and the statistical
» notion that if you keep repeating an event with X probability of success,
» the cumulative probability of success is basically the sum of all the
» individual probabilities. So if you roll a pair of dice 10 times, you have
» a 10X greater chance of getting at least one lucky 7, than if you roll the
» dice only once.
»
»
» » I wonder why Aderans didn’t try follow/up injections at different
» intervals.
»
» I think we don’t know that they didn’t.
In the video presentation they state that they did not.
» Ok then. And thanks for clearling that up. And this makes the idea of
» doing follow-up injections at different intervals with the Aderans
» treatment even more attractive.
» I agree on a lot of that.
»
» But I don’t think Aderans is at so much risk of stopping now. As long as
» they can make a plausible case to their investors that their posted
» phase-II results can be achieved for the average patient, then I think they
» will push forward to market.
Yeah, i’ll be watching Aderans closely. If they go forward with phase III study, then i would say that there is some light at the end of the tunnel. Lets hope that the phase II study results are significantly better than what they’ve shown so far. That 60% responder rate is very distressing. Even if they have something that works well, you’ll still be at the mercy of fate. A coin toss to determine whether you can treat it or not. I can’t imagine what it would be like to have a commercially available treatment that works well only to find out that it won’t work for you. That would be a tough pill to swallow - like being cursed by god. 40% of people who seek treatment from them will feel that way.
What was that 60% figure applying to, anyway? I can’t remember now. Was that for everything they were doing, or just for their most successful protocol to date?
I agree the compounding issue with ARI might change the whole picture. It seems reasonable to think it could be for the better.
» What was that 60% figure applying to, anyway? I can’t remember now. Was
» that for everything they were doing, or just for their most successful
» protocol to date?
»
» I agree the compounding issue with ARI might change the whole picture. It
» seems reasonable to think it could be for the better.
I believe the 60% responder result was presented in the last presentation they put up on line. But I don’t know exactly where that information came from or what protocol generated it. Hopefully it’s not the protocol that they go forward with.
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